Targeting ALDH2 in Atherosclerosis: Molecular Mechanisms and Therapeutic Opportunities

Ma, Sai; Cao, Feng

doi:10.1007/978-981-13-6260-6_12

Cited by 5 publications

(4 citation statements)

References 50 publications

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“…Atherosclerosis is an age-related pathophysiological process that eventually leads to various cardiovascular diseases. Growing evidence from both clinical and basic research has confirmed an association between ALDH2 and atherosclerosis [39] . Stachowicz et al and Lapenna et al reported an inverse relationship between ALDH2 activation and atherosclerosis severity [40,41] .…”

Section: Aldh2 and Atherosclerotic Diseasesmentioning

confidence: 99%

“…For example, meta-analyses have revealed that the ALDH2 ∗ 2 allele is associated with low HDL-C levels in East Asians [46] and that the ALDH2 genotype is associated with blood pressure in both Chinese and Japanese cohorts [38,47] . These findings indicate that ALDH2 may reduce the progression of atherosclerosis by regulating lipid profiles and blood pressure [39] . In contrast, a study that surveyed a Han Chinese cohort reported that ALDH2 mutations (ALDH2 ∗ 1 or ALDH2 ∗ 2 ) are not related to coronary atherosclerosis severity [48] ; however, other risk factors may have caused this discrepancy in results.…”

Section: Aldh2 and Atherosclerotic Diseasesmentioning

confidence: 99%

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Aldehyde dehydrogenase 2-associated metabolic abnormalities and cardiovascular diseases: current status, underlying mechanisms, and clinical recommendations

Cui

Chen

et al. 2022

Cardiology Plus

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Cardiovascular diseases originate from various pathogeneses, among which metabolic abnormalities are common. An integrated metabolic disturbance in common cardiovascular diseases has been suggested, particularly in the Asian population. This speculation is supported by the finding that aldehyde dehydrogenase 2 (ALDH2) gene mutations are present in nearly half of the Asian population. ALDH2 mutations significantly reduce ALDH2 enzyme activity and increase production of toxic aldehydes, including 4-hydroxynonenal, and are involved in the pathophysiology of several cardiovascular disorders such as atherosclerosis and myocardial infarction. Additionally, individuals with ALDH2 mutations are more susceptible to hypertension and diabetes, and these mutations are significantly correlated with heart failure. Until now there are no actionable clinical recommendations with regards to screening for ALDH2 mutations. A comprehensive understanding of the relationship between ALDH2 and these etiologies may greatly help in better prevention and treatment of cardiovascular diseases in populations, especially Asian, where ALDH2 mutations are common.

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Section: Aldh2 and Atherosclerotic Diseasesmentioning

confidence: 99%

Section: Aldh2 and Atherosclerotic Diseasesmentioning

confidence: 99%

Aldehyde dehydrogenase 2-associated metabolic abnormalities and cardiovascular diseases: current status, underlying mechanisms, and clinical recommendations

Cui

Chen

et al. 2022

Cardiology Plus

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“…The molecular mechanism of atherosclerosis involves multiple pathways at the molecular level. [6,7] Functional analyses have shown that some factors can be targeted to improve atherosclerosis therapy. [8] It is known that long noncoding RNAs (lncRNAs) and micro RNAs (miRNAs) are involved in various human diseases including atherosclerosis.…”

Section: Introductionmentioning

confidence: 99%

LncRNA MCM3AP-AS1 is downregulated in atherosclerosis and sponges miR-448 to suppress vascular smooth muscle cell proliferation

Liu

Qin

2023

Medicine

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Long noncoding RNA MCM3AP-AS1 plays critical roles in cancers, but its role in atherosclerosis is yet to be elucidated. The expression of MCM3AP-AS1 in atherosclerosis and control plasma samples were measured by RT-qPCR. IntaRNA was used to predict potential base pairings between MCM3AP-AS1 and miR-448, and the results were confirmed by a dual luciferase activity assay. Cell proliferation assay was performed to explore the role of overexpression of MCM3AP-AS1, miR-448, and myocyte enhancer factor 2 (MEF2)-C in the proliferation of human aortic smooth muscle cells (HAOSMCs). MCM3AP-AS1 was downregulated in atherosclerosis and directly interacted with miR-448, which is a critical player in the proliferation of HAOSMCs, indicating its involvement in atherosclerosis. However, MCM3AP-AS1 and miR-448 showed no role in regulating the expression of each other. In contrast, overexpression of MCM3AP-AS1 increased the expression levels of MEF2-C, which can be targeted by miR-448. Moreover, MCM3AP-AS1 was found to inhibit the effects of miR-448 overexpression on both HAOSMC proliferation and MEF2-C expression. MCM3AP-AS1 is downregulated in atherosclerosis and sponges miR-448 to suppress the proliferation of HAOSMCs.

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“…6,7 The mechanisms and functions of ALDH2 in heart failure, atherosclerosis, ischemic cardiomyopathy, and alcoholic heart disease have been previously reported, indicating that ALDH2 is a cardioprotective enzyme. [6][7][8][9][10] After phosphorylation, the increase in ALDH2 activity prevents arrhythmias via related mechanisms. 11,12 In this review, we summarize the potential mechanisms underlying the beneficial effects of ALDH2 activation in attenuating arrhythmias, the increased risk of arrhythmogenesis in individuals with the inactive ALDH2 rs671 polymorphism, and possible future research directions with respect to ALDH2 activation in arrhythmia treatments.…”

Section: Introductionmentioning

confidence: 99%

Aldehyde dehydrogenase 2 and arrhythmogenesis

2022

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Targeting ALDH2 in Atherosclerosis: Molecular Mechanisms and Therapeutic Opportunities

Cited by 5 publications

References 50 publications

Aldehyde dehydrogenase 2-associated metabolic abnormalities and cardiovascular diseases: current status, underlying mechanisms, and clinical recommendations

Aldehyde dehydrogenase 2-associated metabolic abnormalities and cardiovascular diseases: current status, underlying mechanisms, and clinical recommendations

LncRNA MCM3AP-AS1 is downregulated in atherosclerosis and sponges miR-448 to suppress vascular smooth muscle cell proliferation

Aldehyde dehydrogenase 2 and arrhythmogenesis

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